cardiac muscles; the heart as a pump and function of valve Flashcards
cardia rhythmicity
trasmiting action potentais through the cardiac muscles to cause the hearts rhythmical beat
three types of cardiac muscles
- atrial muscles
- ventricle muscles
- excitatory and conductive muscle fiber
how excitatory and conductive fibers contract?
the contract by automatic rhythmical electrical discharge in the form of action potential or conduction of action potential by the heart that creates an excitatory system that controls the systematic beating of the heart
Explain left ventricle rotation
the left ventricle twists during a systole . It has muscle fiber layers. The subepicardial (outer) layer spirals towards right and the subendocardial (inner) spirals towards the left which causes the apex of the heart to move clockwise and the base to move anticlockwise
During systole the ventricle moves downwards the apex and after systole it recoils untwist during relaxation diastole
Cardiac muscle is a syncytium
the cells if cardiac muscles are joined together by intercalated disks. These intercalated disk join the cardiomyocytes by making a permeable connection between the cells (gap junction). The ions move across this junction to neighbouring cells which also allows action potential to move across each cell. Cardiac muscle is a syncytium of many heart cells that are so interconnected that when one cell gets excited all the cells receives the action potential
two syncytia
atrial syncytia and ventricle syncytia
What separatees atrium and ventricle
fibrous tissue that surround the atrioventricular valve.
how action potential spreads from atria to ventrucle
by AV bundle
Action potential recorded in ventricle
stays about average of 105 millivolts. Intracellular potential goes from a negative between beats of -85 millivolt to positive of +20 millivolt. After spike the membrane remains depolarized for 0.2 secs, and repolarizes again.
Causes of long action potential in cardia muscles
- Contains slow calcium channels, which open late and then remain open for a tenth of a second intitiates the contraction.
- Immediately after the onset of a action potential the permeability of positive K ions decrease by five fold, which stops the efflux of +vely charged K ions during action potential and prevents early return of action potential to its normal level
Phase 0
Cardiac cell stimulated and depolarizes, making the action potential positive to 20millivolts. Voltage gated fast sodium channels open and Na efflux increases
Phase 1
initial repolarization- Na channels close and potassium leaves the cell
phase 2
initial repolarization occurs and then action potential plateaus causes of increase calcium permeability and decrease K permeability. The Ca channels open at phase 0 &1 and potassium channels close, which stops the efflux of K ions to the outside
Phase 3
opening of K channels causes efflux of K ions and closing of Ca channels and cello membrane return to normal action potential
Phase 4
resting membrane potential averages about -80to -90
Velocity if signal conduction in heqrt
0.3 to 0.5 m/sec which is 1/250 the velocity of a large nerve fiber and 1/10 of a skeletal muscle. 4m/sec in purkinjee fiber
refractory period ?
it is the interval of time in which the cardiac impulse cannot re excite an already excited cardiac muscle
Values of refractory period
- 25-0.30 second for ventricles
0. 15 for atrial
Relative refractory period
Addition 0.05 second during which an excited muscle is more Hard to re-excite but it can still be re excited with a very strong excitation signal
Explain the process of excitation that happens in same way in skeletal ma
he action potential reaches the the interior of cardiac muscles, from there jt travels to the membranes of longitudinal T tubules then it acts on the membrane of sarcoplasmic tubules which causes the release of calcium ions into the muscle sarcoplasm and in few thousandth of seconds actin and myosin filaments slide over each other to cause muscle contraction
What differently happens in cardiac muscle than in skeletal muscle during muscle contraction
Calcium ions from T tubule also diffuse into the sarcoplasm, which opens the voltage dependant calcium channels in the membrane of T tubule, calcium entering the cell then activates calcium release channels or ryanodine receptors in the sarcoplasmic reticulum triggering the calcium ions to be released in the sarcoplasm
Cardiac cycle
the events from the begging of one heartbeat to the begging of the other is called as cardiac cycle
Explain where cardiac cycle in events
starts from sinus node which is present on the superior lateral wall of right atrium from where the superiors vena cave enters then passes to both atria then to Av bundle and then to ventricles.
Why atria are prime pumpers
there is a delay of more than 0.1 second during the passage of each cardiac impulse from atria to ventricle . So the atria contracts ahead of ventricle
Period of rapid filling of ventricle
During a ventricular systole, large amount of blood accumulate in right and left atrial due to closed AV valve. During ventricle diastole, the pressure inside the ventricles decreases and the already made pressure in the atria during ventricle systole causes the opening of AV Valve and rapidly fills the ventricle with blood
The three thirds of diastole in which the blood fills the ventricle
in healthy humans the period of rapid filling of ventricle lasts for the first third of the diastole. The mid third is when a very small amount of blood passes to ventricles which the the blood coming from veins into the atria and it passes directly into the ventricle. The last third is when the atria contracts and give additional thurst and fills the heart with the 20% of blood to the heart
What happens to people heart disease
In cardiac fibrosis or diabetes mellitus the ventricles stiffen up this causes less blood to fill the ventricles during the early diastoles and require more volume or more filling from later atrial contraction
Period of isovolumic contraction
when the ventricle contracts, it takes 0.2 to 0.3 second to to build up sufficient pressure to push the semilunar valves. In this time contraction is occurring but no emptying is done that is the muscle tension is increasing but no muscle shortening is happening
period of ejection
when the pressure of left ventricle increases more than 80 mm Hg the pressure opens the semilunar valves and the blood goes into the aorta and pulmonary artery. 60% of the blood is ejected at the end of the diastole, 70% is ejected in First third Called period of rapid ejection and the 30% is ejected in the rest of the two thirds called the period of slow ejection
Period of isovolumic relaxation
at the end of systole, ventricle relaxation behinds and the pressure decreases in the ventricles. The aorta and pulmonary artery valves to be closed when the hood in send back because of pressure created in the distended arteries. 0.03 to 0.06 second is taken More by ventricle to relax, even though the volume isn’t changing
End diastolic volume
When the blood enters the ventricle the increase In volume of each of the ventricle is 110 to 120 ml called as end diastolic volume
Stroke volume output
when the ventricles get empty the volume decreases by about 70ml stroke volume output
End systolic volume
remaining volume in each ventricles is 40 to 50ml called end systolic volume
Ejection fraction
the fraction of end diastolic volume that is ejected is 60%. It is clinically used to asses cardiac systolic pumping
where are papillary muscles in the heart are founds
they are attached to the vane of av valves by the chordae tendineae.
Functions of papillary muscles in heart
They papillary muscles contract when the ventricle walls contract, they pull on vanes of the valve pulling them inwards into the ventricle preventing them from bulging too much into the atria
preload
the degree of tension in the muscle when it becomes contracted is pre load
after load
the load against which the muscles exerts the contractile force
basic mechanisms of regulation of heart pumping
- intrinsic cardiac pumping regulation in response to the change in the volume of blood flow
- regulation of heart beat through the autonomic nervous system
Frank sterling mechanism of the heart
the intrinsic ability of heart to manage blood flow is called Frank steeling mechanism of heart. It means the greater the heart muscle is stretched during blood filling, the greater the force of contraction, the greater the quantity of blood flown into aorta
Effect of K ions on hear function
increased level of K ions in extracellular fluid makes the heart dilated and flaccid, also decreases the cardiac impulses travelling from atrial to ventricle through Av node. Only 2-3 times more value than normal of K ions can cause abnormal rhythm and death
Why k ions have that affect
it lowers the membrane potential by causing depolarization, low membrane potential means Low action potential intensity and intensity muscle contraction weakens
Effect of Ca ions
opposite effect to K ions, it causes spastic contractions
